Reactive species and pulmonary edema.
Reactive species and pulmonary edema.
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DOI：
10.1586/ers.09.41
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发表时间：
2009-10-01
影响因子：
3.9
通讯作者：
Matalon S
中科院分区：
文献类型：
--
作者：
Iles KE;Song W;Miller DW;Dickinson DA;Matalon S
当进入肺间质的液体流量超过其排出量时，就会发生肺水肿，导致低氧血症，甚至死亡。非心源性肺水肿(NPE)通常是由于微血管和肺泡对血浆蛋白的通透性增加而引起的，其中一个可能的病因是氧化损伤。活性氧和氮化物(RON)可以改变或破坏离子通道，如上皮钠通道，从而改变液体平衡。在实验系统中，RONS的增加或保护性抗氧化机制的降低会导致上皮钠通道活性的改变，并支持RONS在NPE中起重要作用的假说。需要基础和临床研究来严格确定RONS-NPE的联系和抗氧化治疗(单独或作为β激动剂的补充)改善患者预后的能力。
Pulmonary edema occurs when fluid flux into the lung interstitium exceeds its removal, resulting in hypoxemia and even death. Noncardiogenic pulmonary edema (NPE) generally results when microvascular and alveolar permeability to plasma proteins increase, one possible etiology being oxidant injury. Reactive oxygen and nitrogen species (RONS) can modify or damage ion channels, such as epithelial sodium channels, which alters fluid balance. Experimental systems in which either RONS are increased or protective antioxidant mechanisms are decreased result in alterations of epithelial sodium channel activity and support the hypothesis that RONS are important in NPE. Both basic and clinical studies are needed to critically define the RONS–NPE connection and the capacity of antioxidant therapy (either alone or as a supplement to β-agonists) to improve patient outcome.